Welcome to the International Skeptics Forum, where we discuss skepticism, critical thinking, the paranormal and science in a friendly but lively way. You are currently viewing the forum as a guest, which means you are missing out on discussing matters that are of interest to you. Please consider
registering so you can gain full use of the forum features and interact with other Members. Registration is simple, fast and free! Click here to register today.

It's called the "Healthy Vaccinee Effect" and you can read about it and the poor quality of data along with overall poor performance of influenza vaccines for yourself in Section: Impact of Influenza Vaccination on Influenza-Related Morbidity and Mortality among Persons 65 Years of Age and Older starting on pp. 24.

Este

Yes, I read that. It's merely an assertion and not very convincing without supporting data. In reality, one would need a study with a control group of similar demographics and health profile to reach such a conclusion. Regarding the limitations of meta-analysis, you might want to take a look at THIS.

Yes, I read that. It's merely an assertion and not very convincing without supporting data. In reality, one would need a study with a control group of similar demographics and health profile to reach such a conclusion. Regarding the limitations of meta-analysis, you might want to take a look at THIS.

It is based upon this, not assertion. There is also a citation list at the end of each chapter in the CCIV report. Based upon your citation, perhaps you would like to identify which biases may have entered into the Osterholm et al. meta-analysis. I see some and they don't speak well of what they had to work with. In my estimation, it is taking a lot of mental gymnastics to cling to a dearly-held belief as opposed to critically examining the strongest evidence and seeing the problems. You know, what sceptics should be doing.

ETA:

Quote:

In reality, one would need a study with a control group of similar demographics and health profile to reach such a conclusion.

I forgot to directly address this so sorry for any confusion. You're right, we only have some weak observational data to define this. And you know what? Now that universal vaccination has been recommended, it is now unethical to conduct any trials that would withhold vaccination in order to conclude this. Brilliant.

We found a dose-response relationship where greater increases in vaccine uptake were associated with greater decreases in influenza-associated outcomes for all health care use outcomes for age groups <65 y (all slopes negative, p < 0.001) (Figure 2). For the elderly, the opposite relationship was observed for mortality and hospitalizations, and no relationship was noted for ED use and office visits.

Quote:

However, for older age groups, in particular those ≥75 y, greater incremental increases in vaccine uptake over time were observed in other provinces compared to Ontario, yet among all the outcomes, none of the RR ratios were greater than one. This result is contrary to what one would expect based on the assumption that greater increases in vaccine uptake in those populations should have been associated with greater decreases in outcome rates, and therefore suggests that influenza vaccines may not be as effective in reducing mortality and health care use in older people compared to younger age groups.

The data is sort of all over the place with flu vaccines, and most of the evidence that exists isn't high quality, but one uncontroversial, consistent trend that seems to pop up everywhere is that after age 65, the vaccine becomes increasingly less effective.

The data is sort of all over the place with flu vaccines, and most of the evidence that exists isn't high quality, but one uncontroversial, consistent trend that seems to pop up everywhere is that after age 65, the vaccine becomes increasingly less effective.

That latter citation is quite persuasive. It is interesting to speculate about the degree to which immune system declines are due to documented declines in the ability to absorb important substances like vitamin D, B-12, zinc, etc. and if supplements can be of value.

It is based upon this, not assertion. There is also a citation list at the end of each chapter in the CCIV report. Based upon your citation, perhaps you would like to identify which biases may have entered into the Osterholm et al. meta-analysis. I see some and they don't speak well of what they had to work with. In my estimation, it is taking a lot of mental gymnastics to cling to a dearly-held belief as opposed to critically examining the strongest evidence and seeing the problems. You know, what sceptics should be doing.

ETA:
I forgot to directly address this so sorry for any confusion. You're right, we only have some weak observational data to define this. And you know what? Now that universal vaccination has been recommended, it is now unethical to conduct any trials that would withhold vaccination in order to conclude this. Brilliant.

Este

From the Ontario study:

Quote:

Conclusions
Compared to targeted programs in other provinces, introduction of universal vaccination in Ontario in 2000 was associated with relative reductions in influenza-associated mortality and health care use. The results of this large-scale natural experiment suggest that universal vaccination may be an effective public health measure for reducing the annual burden of influenza.

OK, the evidence does seem to indicate that older people do not benefit as well from the vaccine, but the immunity provided to younger adults and children should work to lessen exposure to the virus for older adults. Would you not agree?

So in all these posts you boil it down to saying all I noted was Osterholm got his flu shot?

But I'll take your cherry picked challenge anyway. Forgive the hi-lights but it seems my posts are not being read. I've made it easier to skim.

Originally Posted by from Este's post, citation?

Last month,, in a step tantamount to heresy in the public health world, scientists at the Center for Infectious Disease Research and Policy at the University of Minnesota released a report saying that influenza vaccinations provide only modest protection for healthy young and middle-age adults, and little if any protection for those 65 and older, who are most likely to succumb to the illness or its complications. Moreover, the report's authors concluded, federal vaccination recommendations, which have expanded in recent years, are based on inadequate evidence and poorly executed studies.

Here's Osterholm's related comments. He is basically saying using a single number for efficacy is not useful. He notes the vaccine and strains and patient factors make using a single average inaccurate. That's great but not practical for public health messages since one wouldn't know that level of detail until after the flu season. Otherwise I have no objection to the conclusion vaccine efficacy is variable. I have said as much several times.

Again, "variable" does not mean, "doesn't ever work".

And we are all aware of the problem with the vaccine use in the elderly. That's why the vaccine formulation now (last 2 flu seasons) being recommended is a higher dose for people over 65. This discussion, however, is about flu in people with no identified risk factors.

Now read Osterholm's second comment in the link. (The copy paste is disabled so you'll need to read it directly.) It's Osterholm explaining his comments have been misinterpreted.

He says we shouldn't oversell the vaccine, but he's not saying not to use the vaccine. You will also note that there is evidence the 60% figure applies to healthy adults under age 65. And Osterholm thinks we need more studies on using the vaccine in healthy kids. That's true for a whole slew of drugs where we have to prescribe for kids based on adult studies because pediatric drug studies are less often done.

All of this is consistent with what I said about the CIDRAP report. They recommend we keep using the vaccine, cut back on the effectiveness estimates and look for better vaccines.

You have to consider research conclusions in the context of provider and researcher philosophies. If you wait for a perfect medicine or perfect research you miss the chance to prevent a lot of disease. When you see a researcher in a blog or study say "we lack consistent evidence", they are not always saying, we have evidence against, or there's not enough evidence to continue a practice.Some benefit and no harm is a reason to continue using a vaccine if it's the only one you have and the disease burden is demonstrated (which it is).

This is the nature of prescribing, and the nature of research and the nature of peer review and meta-analyses. Unfortunately a lot of people reading the studies and comments are not familiar with all these nuances.

The fact remains, Osterholm supports using the fly vaccine. Osterholm has said in multiple links I have cited that he is not saying the vaccine doesn't work or shouldn't be given to healthy people. If anything he's saying giving it to the healthy adults will do the most good.

Originally Posted by Estellea

The pooled efficacy (not effectiveness in one age group was estimated at 59% so please represent that properly. It is not overall efficacy. And in some years with some age and risk groups the vaccine efficacy and effectiveness was absent.

Are you complaining I rounded 59 to 60? Reading Osterholm's comments in the link above says I interpreted the comments correctly whether you think I did or not. I noted the variability in my post and we are talking about vaccinating healthy people under age 65.

Why is a higher dose vaccine available for adults 65 and older?
Human immune defenses become weaker with age, which places older people at greater risk of severe illness from influenza. Also, ageing decreases the body's ability to have a good immune response after getting influenza vaccine. A higher dose of antigen in the vaccine is supposed to give older people a better immune response and therefore better protection against flu.

Does the higher dose vaccine produce a better immune response in adults 65 years and older?
Data from clinical trials comparing Fluzone to Fluzone High-Dose among persons aged 65 years or older indicate that a stronger immune response (i.e. higher antibody levels) occurs after vaccination with Fluzone High-Dose. Whether or not the improved immune response leads to greater protection against influenza disease after vaccination is not yet known. An ongoing study designed to determine the effectiveness of Fluzone High-Dose in preventing illness from influenza compared to Fluzone is expected to be completed in 2014-2015.

OK, the evidence does seem to indicate that older people do not benefit as well from the vaccine, but the immunity provided to younger adults and children should work to lessen exposure to the virus for older adults. Would you not agree?

In age-specific analyses, larger mortality decreases in Ontario were found to be statistically significant only in those ≥85 y.

Quote:

In age-specific analyses, greater decreases were consistently observed in Ontario than other provinces for age groups <65 y. For seniors, greater decreases were observed in Ontario than other provinces for hospitalizations among those aged 65–84 y and for ED use among those 65–74 y.

Quote:

Despite universal availability of publicly insured health care services, enhanced access to free influenza vaccines in Ontario since 2000, and extensive media communications, only an estimated average of 38% of the overall household population reported receiving them during the post-UIIP introduction period. Although vaccine uptake was higher in older age groups (e.g., approximately 80% among those ≥75 y), it is uncertain that levels required for appreciable herd immunity effects were obtained in the overall population, particularly in younger age groups....

...In Ontario, vaccination rates among those aged 12 to 19 y increased from 16% to 31% over the study period, while in other provinces, rates increased from 6% to 11%. We observed more than 50% reductions in both influenza-associated mortality and health care use over the study period among seniors in both Ontario and other provinces. The bulk of these decreases are likely attributable to less severe influenza seasons across Canada in the postintervention period, but the larger observed decreases in mortality for seniors aged ≥85 y, hospitalizations for seniors aged 65–84 y, and ED use for those aged 65–74 y in Ontario compared to other provinces may be compatible with some indirect benefits as previously posited [46]

So vaccination rates were higher in kids in Ontario, in all provinces the degree of flu burden decreased but with several measures Ontario did see a benefit in the elderly with a higher vaccination rate in the kids. Think what might be seen with higher vaccine uptake.

I also wanted to point this out: Flu cases, not the raw ILI and P cases were used:

Quote:

We estimated influenza-associated events using a two-step procedure. We first ran multivariate regression models to estimate weekly events as a function of population and influenza season factors, and used this model to generate an expected baseline representing the pattern of events occurring in the absence of influenza. We then computed influenza-associated events as the difference between the number of observed events and expected baseline events during periods of influenza activity.

OK, the evidence does seem to indicate that older people do not benefit as well from the vaccine, but the immunity provided to younger adults and children should work to lessen exposure to the virus for older adults. Would you not agree?

Theoretically, if the strain match is good and the uptake is high, then we could see a herd effect.

So in all these posts you boil it down to saying all I noted was Osterholm got his flu shot?

Take it as an act of kindness given your arguments from assertion and the fact that you haven't even read the Cochrane Review on Influenza Vaccines and Healthy Adults.

Quote:

But I'll take your cherry picked challenge anyway. Forgive the hi-lights but it seems my posts are not being read. I've made it easier to skim.
Are you quoting the NY Times? I missed your citation.

Here's Osterholm's related comments. He is basically saying using a single number for efficacy is not useful. He notes the vaccine and strains and patient factors make using a single average inaccurate. That's great but not practical for public health messages since one wouldn't know that level of detail until after the flu season. Otherwise I have no objection to the conclusion vaccine efficacy is variable. I have said as much several times.

So you are saying that it's fine to lie to the public. Why would presenting a range of effectiveness for the vaccine in the various groups along with the caveat of strain match "not practical for public health messages"? The excuse that we don't have that information until after the flu season is bollocks. We have decades of flu seasons that have been audited. There is also the problem of cultivating public health policy without the evidence to do such.

Quote:

Again, "variable" does not mean, "doesn't ever work".

Strawman noted.

Quote:

And we are all aware of the problem with the vaccine use in the elderly. That's why the vaccine formulation now (last 2 flu seasons) being recommended is a higher dose for people over 65. This discussion, however, is about flu in people with no identified risk factors.

Then how has a vaccine that has not been shown to be efficacious in that target group been implemented into policy and promoted so heavily? No, this is about "the science not agreeing with the science" and you have been addressing flu vaccine issues that encompass many different groups. You don't get to shift the goalposts because the evidence is inconvenient to your dogma.

Quote:

Now read Osterholm's second comment in the link. (The copy paste is disabled so you'll need to read it directly.) It's Osterholm explaining his comments have been misinterpreted.

He says we shouldn't oversell the vaccine, but he's not saying not to use the vaccine. You will also note that there is evidence the 60% figure applies to healthy adults under age 65. And Osterholm thinks we need more studies on using the vaccine in healthy kids. That's true for a whole slew of drugs where we have to prescribe for kids based on adult studies because pediatric drug studies are less often done.

Another right load of bollocks. The evidence for flu vaccine effectiveness is absent in children and other groups yet policy to vaccinate them was made. This isn't the same as prescription drugs and you should know that. I don't see how you can't see the difference between "not using the vaccine" and seriously over-selling it as you think it applies to me. I take exception to the over-promotion and how policy was implemented. Now don't you think that the public is also onto that and we are seeing a backlash?

Quote:

All of this is consistent with what I said about the CIDRAP report. They recommend we keep using the vaccine, cut back on the effectiveness estimates and look for better vaccines.

That's not all that was said; serious problems were identified surrounding policy promulgation and promotion. Not to mention that the effectiveness evidence is absent in many of the groups the vaccine is recommended for.

Quote:

You have to consider research conclusions in the context of provider and researcher philosophies. If you wait for a perfect medicine or perfect research you miss the chance to prevent a lot of disease. When you see a researcher in a blog or study say "we lack consistent evidence", they are not always saying, we have evidence against, or there's not enough evidence to continue a practice.Some benefit and no harm is a reason to continue using a vaccine if it's the only one you have and the disease burden is demonstrated (which it is).

Don't you, of all people try to lecture me or anyone else on the perfect solution fallacy; none of this is justification for what we have been told. Not having adequate evidence to implement policy and over-promoting a public health measure is no better than having evidence it doesn't work.

Quote:

This is the nature of prescribing, and the nature of research and the nature of peer review and meta-analyses. Unfortunately a lot of people reading the studies and comments are not familiar with all these nuances.

Coming from someone who hasn't even read the studies she is questioning would be laughable if not for being someone in a position of disseminating false and misleading information to the credulous public.

Quote:

The fact remains, Osterholm supports using the fly vaccine. Osterholm has said in multiple links I have cited that he is not saying the vaccine doesn't work or shouldn't be given to healthy people. If anything he's saying giving it to the healthy adults will do the most good.

And the fact remains that we have no good evidence that the vaccines work in the very risk groups who are most vulnerable to serious complications from influenza and only modest average protection in healthy adults when we have been peddled a 70-90% effective range for years for everyone vaccinated.

Quote:

Are you complaining I rounded 59 to 60? Reading Osterholm's comments in the link above says I interpreted the comments correctly whether you think I did or not. I noted the variability in my post and we are talking about vaccinating healthy people under age 65.

No, I'm complaining that you are using the 59% (60%) figure as across-the-board. That is only the pooled efficacy for a single group. I suggest you read the meta-analysis by Osterholm et al. if you are actually interested in representing flu vaccine effectiveness properly that is.

So vaccination rates were higher in kids in Ontario, in all provinces the degree of flu burden decreased but with several measures Ontario did see a benefit in the elderly with a higher vaccination rate in the kids. Think what might be seen with higher vaccine uptake.

I also wanted to point this out: Flu cases, not the raw ILI and P cases were used:

Quote:

We estimated influenza-associated events using a two-step procedure. We first ran multivariate regression models to estimate weekly events as a function of population and influenza season factors, and used this model to generate an expected baseline representing the pattern of events occurring in the absence of influenza. We then computed influenza-associated events as the difference between the number of observed events and expected baseline events during periods of influenza activity.

So tell me SG, what in Hades do you think an "influenza-associated event" is? And what do you think their "observed events" are?

And I love this statement from the same study:

Quote:

A previous study reported that UIIP introduction did not lead to reduced influenza incidence [35], but used numbers of laboratory-confirmed cases as the outcome. Their negative finding may have been a result of ascertainment bias arising from a 10-fold increase in testing for influenza over the study period [36].

Well that's kind of a duh! moment don't you think? It is essentially, an experimental vaccine and the earliest we will see any field data is next year at best. What does that have to do with the many years of promoting a vaccine with outright false and misleading claims?

So much to say, so little time. But I don't believe my question has been answered.

If there are documented cases of people with no identified risk factors dying and being hospitalized from flu infections, (and there are), and you have a vaccine that works at least some of the time, (again we are talking about healthy people, no identified risk factors), how can that combination equal no benefit from the vaccine?

And if you have a vaccine that works some of the time, how does that not benefit susceptible people by stopping at least some of the transmission?

So much to say, so little time. But I don't believe my question has been answered.

If there are documented cases of people with no identified risk factors dying and being hospitalized from flu infections, (and there are), and you have a vaccine that works at least some of the time, (again we are talking about healthy people, no identified risk factors), how can that combination equal no benefit from the vaccine?

Low vaccine effectiveness, low uptake and on a population basis very few influenza-related case fatalities.

Quote:

And if you have a vaccine that works some of the time, how does that not benefit susceptible people by stopping at least some of the transmission?

It can't stop transmission but provide a barrier with a vaccine that has good strain matching and very very high uptake.

If the meta-analyses were predictive, then even a small benefit should be detectable. If you can detect 1.6 excess cases of GBS in 100 million flu vaccine recipients, you should be able to detect 1.6 less fatalities in 100 million healthy people with no identified risk factors who got a flu vaccination.

If the meta-analyses were predictive, then even a small benefit should be detectable. If you can detect 1.6 excess cases of GBS in 100 million flu vaccine recipients, you should be able to detect 1.6 less fatalities in 100 million healthy people with no identified risk factors who got a flu vaccination.

Minor quibble but the estimated risk of GBS/million vaccine doses is 1.6. Yes, we should be able to detect 1.6 survivals per million population of interest. But the Osterholm et al. meta-analysis and the Cochrane Healthy Adult systematic reviews did not include mortality data (yes I know that the Cochrane Review included hospitalisations). The other problem that I have been saying all along is the quality or precision of the data that do estimate influenza morbidity/mortality and vaccine coverage are very poor.

So, rather than start off with all the links, they can be overwhelming, we are talking about hundreds of studies and reviews, I thought I'd just start the discussion and see what people think.

SG- First, I have not read the thread . This is a response to the line above in the OP.
If I repeat what someone already said, sorry.

I think we can't afford to ignore the effect of public perception, which feeds back into government policy, in vaccination programme issues- especially in "social" medicine countries like the UK.
My mother is 86 and entitled to an annual flu vaccination. She took it once, several years ago, reacted badly to it and has never taken it again. Discussing it with her, I learn many of her elderly friends have the same attitude.
In part this is because they have heard thet viruses mutate rapidly and that there is no guarantee that a vaccine devised last year will be effective this year.
I've never had one, in part because I never felt I was in a high risk group - and because I hop from country to country so often I'm likely to catch a virus that is not the one currently being targeted in Britain.
There's also the "negative act" thing- whether it's putting snow tyres on the car or having a vaccination, if the problem does not manifest itself, we don't think "I did well", we think "Well that was a waste of time".
Convincing people that by having a vaccination they contribute to universal health takes work.
Now my perception on this may be very wrong and I'll now go back and read the thread which may educate me, but you sought comment and I guess that's my 2 cents worth.

SG- First, I have not read the thread . This is a response to the line above in the OP.
If I repeat what someone already said, sorry.

I think we can't afford to ignore the effect of public perception, which feeds back into government policy, in vaccination programme issues- especially in "social" medicine countries like the UK.
My mother is 86 and entitled to an annual flu vaccination. She took it once, several years ago, reacted badly to it and has never taken it again. Discussing it with her, I learn many of her elderly friends have the same attitude.
In part this is because they have heard thet viruses mutate rapidly and that there is no guarantee that a vaccine devised last year will be effective this year.
I've never had one, in part because I never felt I was in a high risk group - and because I hop from country to country so often I'm likely to catch a virus that is not the one currently being targeted in Britain.
There's also the "negative act" thing- whether it's putting snow tyres on the car or having a vaccination, if the problem does not manifest itself, we don't think "I did well", we think "Well that was a waste of time".
Convincing people that by having a vaccination they contribute to universal health takes work.
Now my perception on this may be very wrong and I'll now go back and read the thread which may educate me, but you sought comment and I guess that's my 2 cents worth.

Consultation rates for influenza-like illness (ILI) and/or acute respiratory infection (ARI) are increasing in most countries in the WHO European Region. In line with observations in previous seasons, influenza activity appears to be migrating from west to east, with countries in the west possibly having reached peak activity while those in the east show slow increases. Influenza A(H1N1)pdm09 remains predominant with co-circulation of influenza A(H3N2) and type B viruses. The proportion of samples from sentinel and non-sentinel sources testing positive for influenza reached its highest level (49%) so far this season The proportion of severe acute respiratory infection (SARI) cases testing positive for influenza continued to increase, mainly owing to influenza A.

(bolding mine)

So as anyone can see, no one in the field is counting all ILIs as flu and ILIs are clearly a valid indicator of flu activity.

Methods
Primary aggregate H1N1pdm serologic data from each study were stratified in standardized age groups and evaluated based on when sera were collected in relation to national or subnational peak H1N1pdm activity. Seropositivity was assessed using well-described and standardized hemagglutination inhibition (HI titers ≥32 or ≥40) and microneutralization (MN ≥ 40) laboratory assays. The prevalence of cross-reactive antibodies to the H1N1pdm virus was estimated for studies using sera collected prior to the start of the pandemic (between 2004 and April 2009); H1N1pdm cumulative incidence was estimated for studies in which collected both pre- and post-pandemic sera; and H1N1pdm seropositivity was calculated from studies with post-pandemic sera only (collected between December 2009–June 2010).

Conclusions
Our results offer unique insight into the global impact of the H1N1 pandemic and highlight the need for standardization of seroepidemiological studies and for their inclusion in pre-pandemic preparedness plans. Our results taken together with recent global pandemic respiratory-associated mortality estimates suggest that the case fatality ratio of the pandemic virus was approximately 0·02%.

Consultation rates for influenza-like illness (ILI) and/or acute respiratory infection (ARI) are increasing in most countries in the WHO European Region. In line with observations in previous seasons, influenza activity appears to be migrating from west to east, with countries in the west possibly having reached peak activity while those in the east show slow increases. Influenza A(H1N1)pdm09 remains predominant with co-circulation of influenza A(H3N2) and type B viruses. The proportion of samples from sentinel and non-sentinel sources testing positive for influenza reached its highest level (49%) so far this season The proportion of severe acute respiratory infection (SARI) cases testing positive for influenza continued to increase, mainly owing to influenza A.

(bolding mine)

So as anyone can see, no one in the field is counting all ILIs as flu and ILIs are clearly a valid indicator of flu activity.

Not no one but this is a better surveillance. They did use ILIs and ARIs for outpatient surveillance however. I'm curious as to why you emphasised the portion you did.

Serology is going to overestimate disease burden or vaccine efficacy; I would be very careful how this is interpreted.

Este

It would take me ages to look it up again, but I saw one European serology study published around 2010 that was perfect. They took blood samples before the 2009 pandemic flu had hit there yet, and then took them again (from the same people) at the end of the season when it had moved on to Oz or wherever. IIRC, in elementary school aged kids they were finding flu incidences bordering on 50%. (something like 20-fold titre rises, and they were excluding the vaccinated.) At the same time, the incidence of "old" H1N1 was rapidly falling and 2009-H1N1 rapidly increasing proportionately in the same regions.

The authors never mentioned it, but I remember thinking they might have unintentionally documented the mechanism by which new pandemic strains "out compete/replace" old ones.

__________________The whole problem with the world is that fools and fanatics are always so certain of themselves, and wiser people so full of doubts ~ Bertrand Russell

Not no one but this is a better surveillance. They did use ILIs and ARIs for outpatient surveillance however. I'm curious as to why you emphasised the portion you did.

What is it about the concept of an indicator, not a direct measurement are you having trouble grasping? And what is it about direct measurements of detectible influenza within sampled ILIs are you not getting?

I posted the EU flu reports which, just like in the US, include a direct measurement of what percentage of the ILIs are culture confirmed influenza. Jefferson is in Italy. I continue to find overwhelming evidence against his statement that we lack a direct measure of influenza as a percentage of ILIs. I'm still looking for something that explains that blatant falsehood since it's just not credible that he doesn't know ILIs are not a direct count of flu cases.

Originally Posted by Estellea

Serology is going to overestimate disease burden or vaccine efficacy; I would be very careful how this is interpreted.

Este

You are claiming antibody specificity is lacking. Do you have any evidence that is the case? Do you think the researchers did nothing to account for vaccinated vs infected prevalence? Where is your evidence vaccine antibody wasn't controlled for?

The process is a fair bit more sophisticated that you seem to think. For example:

Using a microneutralization assay, we measured cross-reactive antibodies to pandemic H1N1 virus (2009 H1N1) in stored serum samples from persons who either donated blood or were vaccinated with recent seasonal or 1976 swine influenza vaccines.

A total of 4 of 107 persons (4%) who were born after 1980 had preexisting cross-reactive antibody titers of 40 or more against 2009 H1N1, whereas 39 of 115 persons (34%) born before 1950 had titers of 80 or more. Vaccination with seasonal trivalent inactivated influenza vaccines resulted in an increase in the level of cross-reactive antibody to 2009 H1N1 by a factor of four or more in none of 55 children between the ages of 6 months and 9 years, in 12 to 22% of 231 adults between the ages of 18 and 64 years, and in 5% or less of 113 adults 60 years of age or older. Seasonal vaccines that were formulated with adjuvant did not further enhance cross-reactive antibody responses. Vaccination with the A/New Jersey/1976 swine influenza vaccine substantially boosted cross-reactive antibodies to 2009 H1N1 in adults.

The point is, serological analyses of influenza antibodies is extremely specific.

Anonymous blood samples were obtained from clinical laboratories and categorized by decade of birth from 1920-2009. Using hemagglutination-inhibition assays, approximately 100 samples per decade (n= 846) were tested from blood samples drawn on hospital and clinic patients in mid-November and early December 2009. Age specific seroprevalences against pandemic H1N1 (A/California/7/2009) were measured and compared to seroprevalences against H1N1 strains that had previously circulated in the population in 2007, 1957, and 1918. (A/Brisbane/59/2007, A/Denver/1/1957, and A/South Carolina/1/1918). Stored serum samples from healthy, young adults from 2008 were used as a control group (n=100). Seroprevalences against pandemic 2009 H1N1 influenza varied by age group, with children age 10-19 years having the highest seroprevalence (45%), and persons age 70-79 years having the lowest (5%). The baseline seroprevalence among control samples from 18-24 year-olds was 6%. Overall seroprevalence against pandemic H1N1 across all age groups was approximately 21%.

There is an extensive discussion on related antibodies detected and how infection with the pandemic strain was determined. Vaccine was not widely distributed in early Dec 2009 in the US. I was only allowed to give it to health care workers and people with identified risk factors under the age of 65 until much later in the season.

We analysed haemagglutination-inhibition (HI) antibody titres of pre-vaccination sera from pandemic vaccine trials conducted in six countries on four continents to provide an indication of A/CA/07/2009(H1N1)-like influenza seroprevalence in those populations. Among 7,962 subjects, ranging in age from 12 months to over 60 years, the proportions with HI antibody titres ≥40 to the H1N1pnd virus in the period from August to October 2009 were, by country: Costa Rica 26.4%, United States (US) 22.5%, Switzerland 16.9%, Germany 12.6%, Belgium 10.1%, and Japan 5.9%. Age-specific seropositivity rates in the samples were higher in children and adolescents in Costa Rica and in the US than in Europe and in Japan. The low proportion of seropositive children in Europe and Japan suggests that little local viral transmission had occurred in those regions even as late as September and October 2009, while in the US and Costa Rica, the greater proportion of previously infected children and young adults suggested that a significant number of asymptomatic infections had occurred during the first pandemic wave.

It would take me ages to look it up again, but I saw one European serology study published around 2010 that was perfect. They took blood samples before the 2009 pandemic flu had hit there yet, and then took them again (from the same people) at the end of the season when it had moved on to Oz or wherever. IIRC, in elementary school aged kids they were finding flu incidences bordering on 50%. (something like 20-fold titre rises, and they were excluding the vaccinated.) At the same time, the incidence of "old" H1N1 was rapidly falling and 2009-H1N1 rapidly increasing proportionately in the same regions.

The authors never mentioned it, but I remember thinking they might have unintentionally documented the mechanism by which new pandemic strains "out compete/replace" old ones.

I would definitely have more confidence in a study of a fluid population with a sufficient sample size and exclusion of vaccination effects like that.

What is it about the concept of an indicator, not a direct measurement are you having trouble grasping? And what is it about direct measurements of detectible influenza within sampled ILIs are you not getting?

Oh I grasp it just fine, do you? ILIs and ARIs as your example used for outpatient activity is not an adequate indicator of influenza activity given that scores of other pathogens are co-circulating and that influenza has a variable prevalence from year to year. That is why active and passive surveillance with antigen based assays are preferred.

Quote:

I posted the EU flu reports which, just like in the US, include a direct measurement of what percentage of the ILIs are culture confirmed influenza. Jefferson is in Italy. I continue to find overwhelming evidence against his statement that we lack a direct measure of influenza as a percentage of ILIs. I'm still looking for something that explains that blatant falsehood since it's just not credible that he doesn't know ILIs are not a direct count of flu cases.

Since you haven't posted where and in what context Dr. Jefferson made this statement, I can't be expected to comment on it now can I.

Quote:

You are claiming antibody specificity is lacking. Do you have any evidence that is the case? Do you think the researchers did nothing to account for vaccinated vs infected prevalence? Where is your evidence vaccine antibody wasn't controlled for?

You know, when you invoke your self-proclaimed authority, you ultimately reveal that you aren't. For instance, HAI tests are highly subjective and can have a range of specificity of ~30% to ~100% depending upon the assay and reader and they are also not standardised which means that tremendous variability occurs. That doesn't mean they are useless, far from it, it just means we have to be cautious when interpreting and comparing results from them. And as for evidence that investigators didn't control for vaccinees in the study that you didn't read (and neither did I since my uni doesn't carry that subscription and I'm not going to have them order it for me) but it states in the CIDRAP news report that you linked to:

Quote:

In discussing possible limitations of the study, the authors said they found conflicting results when they assessed the potential impact of pH1N1 vaccination on their findings. Because of this, and because vaccine coverage in most countries was low when samples were collected, they believe the vaccine had little impact on their results.

So the answer is no, the authors didn't control for it and nor did they think it impacted their results. I don't know that to be the case without reading the full report and more importantly, neither do you.

Quote:

The process is a fair bit more sophisticated that you seem to think. For example:

Don't know if they included this study in the meta-analysis but it nonetheless describes just how specific the antibody tests are: Seroprevalence Following the Second Wave of Pandemic 2009 H1N1 InfluenzaThere is an extensive discussion on related antibodies detected and how infection with the pandemic strain was determined. Vaccine was not widely distributed in early Dec 2009 in the US. I was only allowed to give it to health care workers and people with identified risk factors under the age of 65 until much later in the season.

I think I know the relative sophistication of various assays and as I said earlier, the specificity is highly variable. And I also added the caveat in an earlier post that care should be taken with interpretation of serological results, not that they were useless.

Now, since you seem to be rather concerned with others derailing your topic, perhaps you would cease to do so yourself. You appear concerned with the Jefferson vaccine effectiveness results. Do you have anything to present with regards to those and why you feel as though they are invalid?

Oh I grasp it just fine, do you? ILIs and ARIs as your example used for outpatient activity is not an adequate indicator of influenza activity given that scores of other pathogens are co-circulating and that influenza has a variable prevalence from year to year. That is why active and passive surveillance with antigen based assays are preferred.

I see, the part you don't get is: THE HEALTH CARE COMMUNITY KNOWS FLU IS ONLY A PERCENTAGE OF ILIS.

Originally Posted by Estellea

Since you haven't posted where and in what context Dr. Jefferson made this statement, I can't be expected to comment on it now can I.

I posted the source, if you didn't look at the context, that's not my fault.

However, I still plan to investigate it further since it is such a bizarre claim given the source should know better.

I see, the part you don't get is: THE HEALTH CARE COMMUNITY KNOWS FLU IS ONLY A PERCENTAGE OF ILIS.

And it isn't a reliable indicator particularly when estimates of the estimates are being made. We have the tech to perform rapid, cheap and accurate assays to better estimate annual, global flu burden. Why dick around with crude data.

Quote:

I posted the source, if you didn't look at the context, that's not my fault.

However, I still plan to investigate it further since it is such a bizarre claim given the source should know better.

I'll get to the rest of you post later.

Then you won't mind posting the source again since you know where to readily find it. That's a really cheap tactic by the way.

And it isn't a reliable indicator particularly when estimates of the estimates are being made. We have the tech to perform rapid, cheap and accurate assays to better estimate annual, global flu burden. Why dick around with crude data.

Viral Circulation Data
Viral circulation data on influenza as well
as other viruses such as respiratory syncytial
virus and rhinovirus may be helpful in an
analysis of influenza’s impact on mortality,
because these viruses often co-circulate with
influenza. The CDC maintains such historical
viral circulation data through programs such
as the National Respiratory and Enteric Virus
Surveillance System. Two attempts were
made to obtain such data for analysis; however, the CDC responded that such data are
only provided on condition of co-authorship,
which I refused.

Is that people previously cultured as flu positive just now coming down with secondary pneumonia and showing up at the hospital, or an antigenic shift decreasing prevalence while increasing severity, or co-infection with something like RSV, or what?

__________________The whole problem with the world is that fools and fanatics are always so certain of themselves, and wiser people so full of doubts ~ Bertrand Russell

And it isn't a reliable indicator particularly when estimates of the estimates are being made. We have the tech to perform rapid, cheap and accurate assays to better estimate annual, global flu burden. Why dick around with crude data.

Claiming it isn't a reliable indicator and your other posts suggest you don't understand what ILIs are an indicator of.

BTW, I'm curious if you can find a record of a significant ILI spike that wasn't accompanied by a significant increase in influenza positive cultures. And I've not looked at Kelly's links yet, but RSV surveillance as well as other viral culture % are also reported during the year. I can check the local lab any time of the year for a breakdown of what they are finding.U of WA Virology lab reports

RSV doesn't tend to show a spike in ILIs like flu does because the majority of the population turning up with ILI symptoms are only a small segment of the population. OTOH, they represent a lot of the viral cultures because sick infants get cultured. The U of WA lab tests all the specimens from the Children's Hospital nearby, as well as a lot of other cultures any of us order in the community.

Originally Posted by Estellea

Then you won't mind posting the source again since you know where to readily find it. [non-productive insult snipped]

Este

I don't mind, the link is on about page 3 or 4.

Gotta walk the dogs and run to the post office and then I'll address a few more things here.

You monitor ILI reports, you see a spike when influenza spikes.
ILI specimens are sampled and cultured. You get the % of ILIs that are influenza.

That's a different number from the virology report. The virology report comes from specimens from sick patients sent to the lab, typically because a very sick patient needs a diagnosis. It's not some random sample of ILIs.

So when you look at RSV surveillance, and the other viruses that are turning up, you are looking at what the lab is finding, mostly from hospitalized patients.

When you look at ILI counts, that is not what the virology lab is sampling.
The CDC tests semi-random samples from ILI specimens taken from sentinel sites to determine the component of ILIs that are influenza.

If you only looked at ILIs in kids under age 2, RSV would account for a large proportion of the specimens. But if you look at all ILIs, RSV will account a small % of the cases.

Sigh, so time consuming to deal with a couple legit experts with illegit beliefs. But, I guess that's why I started the thread. Take this as a partial reply, because if I don't post part of it, I may never finish it.

Epidemiologist Tom Jefferson, MD, author for the independent Cochrane Acute Respiratory Infections Group, suggests the incidence of influenza is greatly inflated because it is systematically confused with influenza-like illness, a syndrome caused in minor part by influenza viruses, but more frequently attributable to other viral and bacterial agents. “Conflation of influenza with influenza-like illness has confused the situation and fueled a frenzy,” he says.

It's an outright lie. He might be conflating what the public and news media confuse for flu, but not the health care community. The more I read from Jefferson, the more I think he's full of his own confirmation bias when it comes dismissing the morbidity and mortality of influenza. I can't find any other explanation for his claims.

Quote:

Experts like Jefferson caution against using the words “flu” and “influenza” interchangeably, noting that “flu” is a more loosely defined category that includes viruses that are not influenza-based, but just happen to cause very similar clinical symptoms.

Yeah, and people think the "stomach flu" is what we're talking about. So what? Health care providers are not the ones making this mistake, at least not on the nurse practitioner/physician level.

Quote:

To illustrate, Jefferson points to Flu Trends (www.google.org/flutrends), a site that estimates flu incidence around the world based on the number of flu-related search queries in each region. “Users of Flu Trends think they are following the spread of influenza,” he notes, “while in reality, the site depicts the spread of influenza-like illness.”

Who cares what's on a Google search for flu? What health care providers or public health professionals use this number?

Once again, it's a friggin correlation, not a raw number or even a direct measurement without additional modifiers.

Quote:

The formal studies are few, but Jefferson has completed calculations based on data from trials for vaccines, and he estimates that, on average, only about 7 percent of those with influenza-like illness actually have influenza.

This is either wrong or misleading, take your pick. Is he completely dismissing the EU and CDC weekly sampling of ILIs? Or is he distorting what CDC and the rest of us mean when we refer to ILIs during flu season. Of course, 7% can be a big number depending on the total ILIs.

Quote:

“The CDC and the media portray influenza as a deadly threat,” he says. “But the data suggest that seasonal influenza is a relatively rare and benign condition, with an incidence not exceeding 1 percent in the general population during autumn and winter months.”

There is OVERWHELMING evidence contradicting this claim.

Quote:

The CDC put the death toll at 36,000 in 2003, though it has recently backed off the claim. “There is no actual body count here, as we have with death by car accident or cancer,” Doshi says. Rather, the numbers are broad estimates, made when the CDC uses statistical modeling to associate “excess deaths” with periods of elevated influenza-virus circulation. “But since there is no guarantee that what they call influenza is actually influenza,” says Doshi, the whole model is unreliable.

I don't think the CDC would agree with this at all. You essentially have dueling experts. I'll look further into Doshi's dismissal of the flu epidemiology models the CDC uses but Doshi implies only one data line goes into the assessment and CDC says they use 7.

You monitor ILI reports, you see a spike when influenza spikes.
ILI specimens are sampled and cultured. You get the % of ILIs that are influenza.

That's a different number from the virology report. The virology report comes from specimens from sick patients sent to the lab, typically because a very sick patient needs a diagnosis. It's not some random sample of ILIs.

So when you look at RSV surveillance, and the other viruses that are turning up, you are looking at what the lab is finding, mostly from hospitalized patients.

When you look at ILI counts, that is not what the virology lab is sampling.
The CDC tests semi-random samples from ILI specimens taken from sentinel sites to determine the component of ILIs that are influenza.

If you only looked at ILIs in kids under age 2, RSV would account for a large proportion of the specimens. But if you look at all ILIs, RSV will account a small % of the cases.

In these 1195 adults with community-acquired pneumonia
admitted during RSV season, the four most commonly identified pathogens were S. pneumoniae (6.2%), influenza virus
types A and B (5.4%), RSV (4.4%), and M pneumoniae
(4.1%). If those with extremely high IgG levels and IgM positive for RSV were included (15 patients), the rate of RSV
infection would be 5.9%. In this study we counted "definite"
infections but not "probable" or "possible" infections; by
these strict criteria, only 21% of the patients had a specific
etiologic agent identified [30]

So among hospitalized adults with pneumonia during ILI season, the % who have confirmed flu and those with RSV are roughly equivalent.

Yes, that's only hospital data, but it's definitely not just kids, and the % positive (among those presumably there for pneumonia or some other severe respiratory issues) exceeds 25% in the peak flu season.

It is implausible that a disease with an "average age of infection" around age one would NOT completely endemic in the adult population.
I think there's just a lack of data n the incidence of RSV in non-hospitalized adults:

Influenza is just one of the respiratory pathogens seen in most winters. Among others respiratory syncytial virus (RSV) is particularly important [35, 36]. RSV appears much more consistently than influenza and in the UK epidemics usually begin in December [37]. However, our understanding of the impact of RSV in adults is very limited because 95% of virological specimens for the investigation of RSV come from children.

__________________The whole problem with the world is that fools and fanatics are always so certain of themselves, and wiser people so full of doubts ~ Bertrand Russell

The people who study the winter respiratory viral epidemics still aren't sure how to interpret the data, so I can't really expect HCPs to be adept at it.

Who are these "people who study ..." and how do you know they don't know how to interpret the weekly influenza surveillance reports showing the % of ILI specimens that are positive for influenza?

You can cite all kinds of unrelated stuff about winter ILIs, none of it says experts aren't sure the influenza surveillance system isn't measuring the % of ILIs that are influenza cases circulating in the sampled population.